Hydrogen Therapy Protects Spinal Cord from Injury in Rats
- Authors
- Jian Tong, Jie Liu, Zhengming Lv
- Journal
- Molecular Biology Reports
- Year
- 2026
- DOI
- 10.1007/s11033-026-11482-x
- Study Type
- Rat
- Outcome
- Positive
- Peer Reviewed
- Yes
- Country
- China
- Health Condition
- Spinal Cord Ischemia-Reperfusion Injury
- Body System
- Nervous System
TL;DR
Hydrogen improved recovery after spinal cord injury by reducing oxidative damage and protecting nerve cells from ferroptosis.
Key Finding
Hydrogen gas treatment significantly improved motor function in rats with spinal cord ischemia-reperfusion injury and reduced markers of oxidative stress and ferroptosis by activating the Nrf2/HO-1 protective pathway in nerve cells.
Summary
This study tested whether hydrogen gas could protect rat spinal cords from damage caused by temporary loss of blood flow followed by blood flow restoration. Researchers found that hydrogen treatment improved movement in injured rats and reduced harmful molecules called free radicals in nerve cells. The hydrogen appeared to work by activating a protective pathway in cells that prevents a type of cell death called ferroptosis (iron-dependent cell damage).
Practical Takeaway
This animal study suggests hydrogen gas may have protective effects against spinal cord injury through antioxidant mechanisms, but these findings are from rats only and have not been tested in humans. Much more research, including human clinical trials, would be needed before hydrogen could be considered a treatment for spinal cord injuries.
Abstract
Purpose: Spinal cord ischemia-reperfusion injury (SCIRI) can lead to significant losses in sensory and motor functions. The precise role of hydrogen (H2) as an antioxidant in the process of ferroptosis is not fully determined. Materials and methods: This study used an abdominal aorta ligation technique to establish a SCIRI model in rats. Following oxygen-glucose deprivation/reoxygenation (OGD/R), HT22 cells were treated with H2 to assess its impact on ferroptosis. Hindlimb motor function was evaluated using the motor deficit index (MDI) and Basso, Beattie, Bresnahan (BBB) scoring, while neuronal damage was assessed via hematoxylin-eosin (HE) and Nissl staining. The DCFH-DA fluorescence probe was used for measuring reactive oxygen species (ROS) production, and mitochondrial membrane potential (MMP) was assessed with JC-1 staining and Tetramethylrhodamine methyl ester (TMRM) staining. Levels of Fe2+, glutathione (GSH), and malondialdehyde (MDA) were quantified using specific assay kits. Protein expressions of ACSL4, GPX4, Nrf2, HO-1, and FTH1 were analyzed via Western blotting. Immunocytochemistry was used to detect Nrf2 and HO-1 expressions. Results: The administration of H2 significantly improved hindlimb motor function in SCIRI rats, concurrently reducing cellular ROS, Fe2+, MDA, and ACSL4 levels. Furthermore, there was an observed increase in FTH1, GSH, and GPX4 levels. Mechanistically, H2 treatment upregulated Nrf2 and HO-1 expression in SCIRI rat spinal cord tissues and in OGD/R-induced HT22 cells. These effects, however, were reversed upon administration of brusatol, an Nrf2 inhibitor. Conclusions: In summary, these findings demonstrate that H2 confers neuroprotection in SCIRI through the activation of the Nrf2/HO-1 signaling pathway and the inhibition of ferroptosis.